HappyPoet wrote:
Hi Dr. Sclafani,
The last case of yours showed how venous blood due to an IJV valvular stenosis on one side can reflux to the Transverse Sinus on the opposite side. I'm curious about refluxed blood that goes even farther--down through the Vertebral Venous system.
As you know, one of Dr. Schelling's theories is that the lowest spinal cord lesion will be at the lowest spinal cord level where such reflux stops. My first spinal lesion was at T5, sensory fibers only, and over the past five years, the lesion has elongated downward through T9, still sensory fibers only (which explains why I am still ambulatory but am in MUCH PAIN).
Per you and IVUS, my Azygos vein is fine, so CCSVI theory doesn't seem to be the explanation for my spinal lesions. I'm wondering if Dr. Schelling's theory explains better than the autoimmune theory or CCSVI theory the primary reason why the lesion grew only downward and did not grow across the cord into motor fibers. What are your thoughts on Dr. Schelling's theory and my thoughts about it?
What imaging modalities can show how far down the Vertebral Venous Plexuses refluxed blood travels?
Thank you!
This has my full attention. As as person PPMS this is the defining question from my point of veiw.
There are so many things that we all want answers for and so little data to guide any insights.
The involvement of the Vertebrals is like the next frontier and I am looking forward to Dr. Zamboni's input here.
It would seem that the rapid re-stenosis of the flow in the IJV's does point to a similar effect as relapse in RRMS.
An underlying insufficiency in other areas being the cause of the continuing progression in any form of MS.
The region of symptom expression (affected area of the body) is linked to the blood flow insufficiency upstream and within the brain at capillary level of blood movement.
The finer points of the symptom expression also lies in the neurological junction points such as the Hypothalamus and Thalamus which can effect multiple sensory and motor systems in a small region of the brain.
The additional factors that make the disease harder to piece together are the co-incidental or mathematical commonalities that occur. The diet, trauma, genetic or hereditary origin, position on the planet lived prior to the age of 15/16 years and many other issues that have been presented and no doubt many more will be linked but not actual cause factors. Most of these factors are the personal make up that will effect the underlying disease mechanism but not be necessary for any one person to be effected by the disease, especially when time is factored into the individual persons disease pattern.
Blood appears to be the most common factor is the disease and in what way it will determine the disease expression is the million dollar question.
Could it be time to focus on individual cases and find the common ground?
Is there enough data being collected by the IRB approved service providers?
Is there enough discussion between IR's to get profiles happening that can be used to learn more?
Is there a need for support for the work the IR's are doing that will collect information that can be used across the centers performing treatments?
Is there research 'people' available to design and define what needs to be collected and followed up?
Are the MS Societies (Internationally) getting on side with the IR's and using the opportunity to advance the knowledge either way?
For those that have been treated is there things that could be fed back to IR's/MS Societies/Neurologists/Researchers any group that can advance the learning?
Most of all I am impressed the effort that Dr. S has made and continues to make for us all. I believe he could be supported better by us the PwMS.
Dr.S and other Dr.s for that matter, is there things we can be doing to help? Or stop doing as well if there are things we need to hear as well?
Nap time, that took 'it' out of me, enjoy your day,
Nigel
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